Pellegrini J J, Horn A K, Evinger C
Department of Biology, College of St. Catherine, St. Paul, MN 55105, USA.
Exp Brain Res. 1995;107(2):166-80. doi: 10.1007/BF00230039.
In this study, we characterized the pathways that generate the trigeminal blink reflex in the guinea pig. Blinks were evoked by stimulation of the supraorbital branch of the trigeminal nerve and measured by recording electromyographic activity in the lid-closing orbicularis oculi muscle (OOemg) and, in one case, lid position. Blinks evoked by stimulation of the supraorbital nerve consisted of two bursts of muscle activity ipsilateral to the side of stimulation. The first, R1, had a latency of 6.9 ms and the second, R2, had a latency of 17.25 ms. Increasing stimulus intensity to 3 times threshold for evoking an ipsilateral blink elicited an R1 and R2 response contralaterally, with latencies of 9.2 ms and 19.25 ms, respectively. We investigated the causes for this bipartite response that is seen in the guinea pig, as well as other mammals including humans. The two-component response could arise from different populations of afferents, or from different central circuits, or a combination of these two causes. Multiunit recording in the trigeminal ganglion and simultaneous measurement of the OOemg showed that activation of A beta afferents alone was sufficient to elicit both the R1 and the R2 responses, but that activation of A delta afferents could enhance both responses. Different neural circuits, however, produce the R1 and R2 responses. Transganglionic tracing with wheatgerm agglutin or choleragenoid subunit of cholera toxin bound to HRP revealed that primary afferents from the supraorbital branch of the trigeminal nerve terminated densely in the dorsal horn of spinal cord segment C1 and in the caudalis-interpolaris border region of the spinal trigeminal nucleus. Injections of HRP into the orbicularis oculi motoneuron region of the facial nucleus showed that both of these regions projected to the facial nucleus. Hemisections at the level of C1 eliminated the R2 blink response, but not the R1 response, evoked by stimulation of the supraorbital branch of the trigeminal nerve. Subsequent hemisections at the level of the obex eliminated the R1 response. Microinjections of the GABAB agonist baclofen into the spinal trigeminal nucleus at the level of the obex abolished the R1 but not the R2 response. Thus, the spinal trigeminal nucleus produces the R1 component, whereas the R2 component originates in the C1 region of the spinal cord.
在本研究中，我们对豚鼠三叉神经眨眼反射的产生途径进行了特征描述。通过刺激三叉神经眶上支诱发眨眼，并通过记录眼轮匝肌（OOemg）的肌电图活动来测量眨眼情况，在一个案例中还测量了眼睑位置。刺激眶上神经诱发的眨眼由刺激侧同侧的两阵肌肉活动组成。第一阵，即R1，潜伏期为6.9毫秒，第二阵，即R2，潜伏期为17.25毫秒。将刺激强度增加到诱发同侧眨眼阈值的3倍时，会在对侧诱发R1和R2反应，潜伏期分别为9.2毫秒和19.25毫秒。我们研究了豚鼠以及包括人类在内的其他哺乳动物中出现这种二分反应的原因。这种双成分反应可能源于不同的传入神经群体，或不同的中枢回路，或这两种原因的组合。在三叉神经节进行多单位记录并同时测量OOemg表明单独激活Aβ传入神经足以诱发R1和R2反应，但激活Aδ传入神经可增强这两种反应。然而，不同的神经回路产生R1和R2反应。用与辣根过氧化物酶结合的麦胚凝集素或霍乱毒素的霍乱毒素亚单位进行跨神经节追踪显示，三叉神经眶上支的初级传入神经在脊髓C1节段的背角和三叉神经脊髓核的尾侧 - 极间边界区域密集终止。将辣根过氧化物酶注射到面神经核的眼轮匝肌运动神经元区域表明这两个区域都投射到面神经核。在C1水平进行半横断消除了刺激三叉神经眶上支诱发的R2眨眼反应，但未消除R1反应。随后在闩部水平进行半横断消除了R1反应。在闩部水平将GABAB激动剂巴氯芬微量注射到三叉神经脊髓核中消除了R1反应，但未消除R2反应。因此，三叉神经脊髓核产生R1成分，而R2成分起源于脊髓的C1区域。
